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Treatment and the treatment process

AML subtypes

Acute myeloid leukemia (AML) is not a single disease but a group of many subtypes. This topic explains how the subtype is identified and why it matters.

Last updated: ~2 min read
On a dark navy background, a glowing tree grows from one stem cell, its branches ending in clusters of differently coloured cells.
Figure 1.AML is a group of several subtypes.

01Short answer

AML subtypes are defined mainly by genetic changes in the leukemia cells. The World Health Organization (WHO) classification first separates AML with defining genetic changes, such as PML::RARA (APL), RUNX1::RUNX1T1, CBFB::MYH11, NPM1 mutation and others. Next come AML related to myelodysplasia and AML after previous treatment. The older FAB classification (M0–M7) was based on how cells look under the microscope and is still sometimes used. The subtype shapes the risk group, the choice of treatment and the use of targeted drugs.

02Simple explanation

Why are they different? A leukemia cell can arise from different genetic "faults". Each gives the disease its own features.

Microscope. The doctor looks at the shape and appearance of the cells.

Flow cytometry. Markers on the cell surface show the cell type.

Genetics. Chromosome and gene tests identify the exact subtype and risk.

03Scientific explanation

WHO classification (5th edition, 2022): groups AML by defining genetic changes (PML::RARA, RUNX1::RUNX1T1, CBFB::MYH11, KMT2A, NPM1, CEBPA and others) and by differentiation. The International Consensus Classification (ICC) is used in parallel.

Risk groups (ELN 2022): genetics define favourable, intermediate and adverse risk. For example, an NPM1 mutation without FLT3-ITD is usually favourable, while a TP53 mutation and a complex karyotype are adverse.

Targets: FLT3, IDH1 and IDH2 mutations and the CD33 marker guide the choice of targeted drugs.

04What happens in the body?

Old and new classification

The FAB system (M0–M7) was based on cell appearance: for example, M3 is APL, and M4 and M5 are monocytic types. Today the main classification is based on genetics, because it better explains how the disease behaves.

Immature blood cells of different shapes and granules in purple-pink tones.
Figure 3.Under the microscope, subtypes can look different.

Genetic changes

Sometimes two chromosomes swap pieces (a translocation) and a new fusion gene forms. Sometimes a single gene is mutated. These changes define both the subtype and the response to treatment.

Pairs of chromosomes on a dark background, two exchanging glowing segments.
Figure 2.Chromosomes swapping pieces can define the subtype.

What does this mean for me?

The subtype helps decide treatment intensity, the need for a transplant and targeted drugs. But the outlook depends not only on the subtype, but also on age, general health and response to treatment.

05How is the subtype identified?

A simplified path from diagnosis to plan.

Sample — Blood and bone marrow.1SampleBlood and bone marrow.
Immunophenotype — Flow cytometry.2ImmunophenotypeFlow cytometry.
Genetics — Chromosome and gene tests.3GeneticsChromosome and gene tests.
Discussion — Risk group and plan.4DiscussionRisk group and plan.
SubtypeThe exact name.
RiskFavourable, intermediate, adverse.
PlanPersonal treatment.

06Some AML subtypes (simplified)

SubtypeFeatureWhy it matters
APL (PML::RARA)t(15;17) translocationSpecial treatment: ATRA + arsenic trioxide
Core binding factor AMLRUNX1::RUNX1T1 or CBFB::MYH11Usually favourable risk
AML with NPM1 mutationCommonOften favourable without FLT3-ITD
FLT3-mutatedA target existsAn FLT3 inhibitor may be added
TP53-mutatedHarder to treatAdverse risk
Myelodysplasia-relatedEarlier blood disorderThe plan may differ

* Not a complete list; only tests can identify the exact subtype.

07Key terms

Subtype
A form of the disease defined by its features.
Translocation
Two chromosomes swapping pieces.
Mutation
A change in a gene.
Karyotype
The overall picture of the chromosomes.
FAB
An older classification based on cell appearance.
Risk group
A group of expected course based on genetics.

08Key points

  • AML includes many subtypes.
  • Today the main criterion is genetics.
  • APL needs special treatment.
  • The subtype affects risk and plan.
  • Some results take several days.
  • The outlook does not depend on subtype alone.

09Frequently asked questions

How is my subtype written in the report?

Usually by the name of the genetic change (for example, "AML with NPM1 mutation"). Ask your doctor to explain.

Can the subtype change over time?

New mutations can appear at relapse, so tests are sometimes repeated.

Does the FAB number still matter?

It is supporting information; key decisions are based on genetics.

Is the subtype inherited?

In most cases the changes are only in the leukemia cells and are not inherited; rare inherited predispositions exist.

10Questions for your doctor

Take these questions to your appointment. The ones you save are collected on the “My questions” page and stay on this device only.

  1. How is my subtype written in the report?

  2. Can the subtype change over time?

  3. Does the FAB number still matter?

  4. Is the subtype inherited?

My questions

12Sources

  1. National Cancer Institute (NCI). Adult Acute Myeloid Leukemia Treatment (PDQ) – Patient Version
  2. American Cancer Society. Acute Myeloid Leukemia (AML) Subtypes and Prognostic Factors
  3. Cancer Research UK. Types and risk groups of acute myeloid leukaemia (AML)
  4. Blood Cancer United (LLS). Acute myeloid leukemia (AML) diagnosis and subtypes
  5. WHO / IARC. WHO Classification of Haematolymphoid Tumours, 5th edition
  6. MedlinePlus. Acute myeloid leukemia
  7. American Cancer Society. Chemotherapy
  8. American Cancer Society. Chemo Infusions or Injections
  9. American Cancer Society. Chemotherapy Side Effects
  10. American Cancer Society. Chemotherapy for Acute Myeloid Leukemia (AML)
Medical disclaimerThis information is for educational purposes only and does not replace medical advice.
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